Brain Cancer

Brain tumors, uncontrolled cellular growth in the cranium or spinal column, arise from any of the cell types found in the brain, such as neurons, glial cells, astrocytes, or cells of the meninges. For example, gliomas are a glial cell cancer, whereas meningiomas are a cancer of the meninges. Each brain cancer form has a specific pathogenesis, with common forms of genetic dysregulation. Recent work demonstrates that activation of certain signaling pathways may be critical for the initiation and progression of brain cancer. For example, by attenuating gene expression, miRNA regulate many biological functions, and some have known oncogenic properties. Although expression studies of different brain tumor types have identified dysregulated miRNA, few are functionally linked to pathogenic mechanisms. Research into the functional consequences of dysregulated signaling pathways and miRNA dysfunction during neurocarcinogenesis may yield insights into the molecular mechanisms behind the pathogenesis of brain tumors. Chronic activation of signaling pathways such as phosphatidylinositol 3-kinase and Ras–MAPK contributes to glioma formation and progression. Activated hedgehog signaling as well as DNA ligase IV and p53 defects are associated with formation of medulloblastoma. Dysregulation of miRNA, such as those in the miR-17-92 cluster have been linked to oncogenesis. Analyzing the expression, regulation, and sequence of brain cancer genes can help determine their relative importance to the biology of the cellular or disease processes under study and further explore the their roles in cell biology. ...

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Brain tumors, uncontrolled cellular growth in the cranium or spinal column, arise from any of the cell types found in the brain, such as neurons, glial cells, astrocytes, or cells of the meninges. For example, gliomas are a glial cell cancer, whereas meningiomas are a cancer of the meninges. Each brain cancer form has a specific pathogenesis, with common forms of genetic dysregulation. Recent work demonstrates that activation of certain signaling pathways may be critical for the initiation and progression of brain cancer. For example, by attenuating gene expression, miRNA regulate many biological functions, and some have known oncogenic properties. Although expression studies of different brain tumor types have identified dysregulated miRNA, few are functionally linked to pathogenic mechanisms. Research into the functional consequences of dysregulated signaling pathways and miRNA dysfunction during neurocarcinogenesis may yield insights into the molecular mechanisms behind the pathogenesis of brain tumors. Chronic activation of signaling pathways such as phosphatidylinositol 3-kinase and Ras–MAPK contributes to glioma formation and progression. Activated hedgehog signaling as well as DNA ligase IV and p53 defects are associated with formation of medulloblastoma. Dysregulation of miRNA, such as those in the miR-17-92 cluster have been linked to oncogenesis. Analyzing the expression, regulation, and sequence of brain cancer genes can help determine their relative importance to the biology of the cellular or disease processes under study and further explore the their roles in cell biology.